It is increasingly being recognized that many diseases present in a sexually dimorphic manner, including endocrinological, inflammatory and (cardio)metabolic diseases. The difference in incidence and severity of disease between males and females can in part be attributed to a different genetic landscape (allosomes), by sex-specific expression of disease-modulators and by the different levels of sex hormones. Nevertheless, there remains a lack of insight in how these factors influence the pathogenesis of diseases. Also, the contribution of steroid hormones to sexual dimorphism warrants more research.
Steroid hormones like androgens, estrogens and glucocorticoids have a similar structure, their receptors are of common ancestry, and their DNA-binding sites are similar or even identical. It is therefore plausible that the signaling pathways of steroid hormones interact, and this is in fact widely described in hormone-driven cancers but understudied in (cardio)metabolic disease and auto-immune disease.
This research topic aims to bring together research on sexual dimorphism and steroid hormone crosstalk, in order to generate a timely overview ranging from molecular, functional, and clinical research. Potential topics include but are not limited to the following:
• Sexual dimorphism in the incidence and severity of endocrinological and metabolic diseases
• Molecular modes of nuclear receptor crosstalk between the GR, MR, AR, ER and PR.
• Different levels of steroid hormone crosstalk including enzymatic (in)activation of hormones, hormone secretion, localization, other indirect modes of interaction
• Translational relevance of steroid hormone crosstalk to human disease (cardiometabolic disease, auto-immune disease, cancer)
It is increasingly being recognized that many diseases present in a sexually dimorphic manner, including endocrinological, inflammatory and (cardio)metabolic diseases. The difference in incidence and severity of disease between males and females can in part be attributed to a different genetic landscape (allosomes), by sex-specific expression of disease-modulators and by the different levels of sex hormones. Nevertheless, there remains a lack of insight in how these factors influence the pathogenesis of diseases. Also, the contribution of steroid hormones to sexual dimorphism warrants more research.
Steroid hormones like androgens, estrogens and glucocorticoids have a similar structure, their receptors are of common ancestry, and their DNA-binding sites are similar or even identical. It is therefore plausible that the signaling pathways of steroid hormones interact, and this is in fact widely described in hormone-driven cancers but understudied in (cardio)metabolic disease and auto-immune disease.
This research topic aims to bring together research on sexual dimorphism and steroid hormone crosstalk, in order to generate a timely overview ranging from molecular, functional, and clinical research. Potential topics include but are not limited to the following:
• Sexual dimorphism in the incidence and severity of endocrinological and metabolic diseases
• Molecular modes of nuclear receptor crosstalk between the GR, MR, AR, ER and PR.
• Different levels of steroid hormone crosstalk including enzymatic (in)activation of hormones, hormone secretion, localization, other indirect modes of interaction
• Translational relevance of steroid hormone crosstalk to human disease (cardiometabolic disease, auto-immune disease, cancer)